177 research outputs found

    Standardization and other approaches to meta-analyze differences in means.

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    Meta-analysts often use standardized mean differences (SMD) to combine mean effects from studies in which the dependent variable has been measured with different instruments or scales. In this tutorial we show how the SMD is properly calculated as the difference in means divided by a between-subject reference-group, control-group, or pooled pre-intervention SD, usually free of measurement error. When combining mean effects from controlled trials and crossovers, most meta-analysts have divided by either the pooled SD of change scores, the pooled SD of post-intervention scores, or the pooled SD of pre- and post-intervention scores, resulting in SMDs that are biased and difficult to interpret. The frequent use of such inappropriate standardizing SDs by meta-analysts in three medical journals we surveyed is due to misleading advice in peer-reviewed publications and meta-analysis packages. Even with an appropriate standardizing SD, meta-analysis of SMDs increases heterogeneity artifactually via differences in the standardizing SD between settings. Furthermore, the usual magnitude thresholds for standardized mean effects are not thresholds for clinically important differences. We therefore explain how to use other approaches to combining mean effects of disparate measures: log transformation of factor effects (response ratios) and of percent effects converted to factors; rescaling of psychometrics to percent of maximum range; and rescaling with minimum clinically important differences. In the absence of clinically important differences, we explain how standardization after meta-analysis with appropriately transformed or rescaled pre-intervention SDs can be used to assess magnitudes of a meta-analyzed mean effect in different settings.fals

    The Hydrating Effects of Hypertonic, Isotonic and Hypotonic Sports Drinks and Waters on Central Hydration During Continuous Exercise: A Systematic Meta-Analysis and Perspective

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    Background Body-fluid loss during prolonged continuous exercise can impair cardiovascular function, harming performance. Delta percent plasma volume (dPV) represents the change in central and circulatory body-water volume and therefore hydration during exercise; however, the effect of carbohydrate–electrolyte drinks and water on the dPV response is unclear. Objective To determine by meta-analysis the effects of ingested hypertonic (> 300 mOsmol kg−1), isotonic (275–300 mOsmol kg−1) and hypotonic (< 275 mOsmol kg−1) drinks containing carbohydrate and electrolyte ([Na+] < 50 mmol L−1), and non-carbohydrate drinks/water (< 40 mOsmol kg−1) on dPV during continuous exercise. Methods A systematic review produced 28 qualifying studies and 68 drink treatment effects. Random-effects meta-analyses with repeated measures provided estimates of effects and probability of superiority (p+) during 0–180 min of exercise, adjusted for drink osmolality, ingestion rate, metabolic rate and a weakly informative Bayesian prior. Results Mean drink effects on dPV were: hypertonic − 7.4% [90% compatibility limits (CL) − 8.5, − 6.3], isotonic − 8.7% (90% CL − 10.1, − 7.4), hypotonic − 6.3% (90% CL − 7.4, − 5.3) and water − 7.5% (90% CL − 8.5, − 6.4). Posterior contrast estimates relative to the smallest important effect (dPV = 0.75%) were: hypertonic-isotonic 1.2% (90% CL − 0.1, 2.6; p+ = 0.74), hypotonic-isotonic 2.3% (90% CL 1.1, 3.5; p+ = 0.984), water-isotonic 1.3% (90% CL 0.0, 2.5; p+ = 0.76), hypotonic-hypertonic 1.1% (90% CL 0.1, 2.1; p+ = 0.71), hypertonic-water 0.1% (90% CL − 0.8, 1.0; p+ = 0.12) and hypotonic-water 1.1% (90% CL 0.1, 2.0; p+ = 0.72). Thus, hypotonic drinks were very likely superior to isotonic and likely superior to hypertonic and water. Metabolic rate, ingestion rate, carbohydrate characteristics and electrolyte concentration were generally substantial modifiers of dPV. Conclusion Hypotonic carbohydrate–electrolyte drinks ingested continuously during exercise provide the greatest benefit to hydration

    High-speed fixed-target serial virus crystallography

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    We report a method for serial X-ray crystallography at X-ray free-electron lasers (XFELs), which allows for full use of the current 120-Hz repetition rate of the Linear Coherent Light Source (LCLS). Using a micropatterned silicon chip in combination with the high-speed Roadrunner goniometer for sample delivery, we were able to determine the crystal structures of the picornavirus bovine enterovirus 2 (BEV2) and the cytoplasmic polyhedrosis virus type 18 polyhedrin, with total data collection times of less than 14 and 10 min, respectively. Our method requires only micrograms of sample and should therefore broaden the applicability of serial femtosecond crystallography to challenging projects for which only limited sample amounts are available. By synchronizing the sample exchange to the XFEL repetition rate, our method allows for most efficient use of the limited beam time available at XFELs and should enable a substantial increase in sample throughput at these facilities

    The Road to the Beijing Winter Olympics and Beyond: Opinions and Perspectives on Physiology and Innovation in Winter Sport

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    Open Access This article is licensed under a Creative Commons Attri bution 4.0 International License, which permits use, sharing, adapta tion, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/Beijing will host the 2022 Winter Olympics, and China strengthens research on various aspects to allow their athletes to compete successfully in winter sport. Simultaneously, Government-directed initiatives aim to increase public participation in recreational winter sport. These parallel developments allow research to advance knowledge and understanding of the physiological determinants of performance and health related to winter sport. Winter sport athletes often conduct a substantial amount of training with high volumes of low-to-moderate exercise intensity and lower volumes of high-intensity work. Moreover, much of the training occur at low ambient temperatures and winter sport athletes have high risk of developing asthma or asthma-related conditions, such as exercise-induced bronchoconstriction. The high training volumes require optimal nutrition with increased energy and dietary protein requirement to stimulate muscle protein synthesis response in the post-exercise period. Whether higher protein intake is required in the cold should be investigated. Cross-country skiing is performed mostly in Northern hemisphere with a strong cultural heritage and sporting tradition. It is expected that innovative initiatives on recruitment and training during the next few years will target to enhance performance of Chinese athletes in classical endurance-based winter sport. The innovation potential coupled with resourcing and population may be substantial with the potential for China to become a significant winter sport nation. This paper discusses the physiological aspects of endurance training and performance in winter sport highlighting areas where innovation may advance in athletic performance in cold environments. In addition, to ensure sustainable development of snow sport, a quality ski patrol and rescue system is recommended for the safety of increasing mass participation

    Oxidation of independent and combined ingested galactose and glucose during exercise.

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    Coingestion of glucose and galactose has been shown to enhance splanchnic extraction and metabolism of ingested galactose at rest; effects during exercise are unknown. This study examined whether combined ingestion of galactose and glucose during exercise enhances exogenous galactose oxidation. Fourteen endurance-trained male and female participants [age, 27 (5) yr; V̇o2peak, 58.1 (7.0) mL·kg−1·min−1] performed cycle ergometry for 150 min at 50% peak power on four occasions, in a randomized counterbalanced manner. During exercise, they ingested beverages providing carbohydrates at rates of 0.4 g.min−1 galactose (GAL), 0.8 g.min−1 glucose (GLU), and on two occasions 0.8 g.min−1 total galactose-glucose (GAL + GLU; 1:1 ratio). Single-monosaccharide 13C-labeling (*) was used to calculate independent (GAL, GLU, GAL* + GLU, and GAL + GLU*) and combined (GAL* + GLU*, COMBINE) exogenous-monosaccharide oxidation between exercise. Plasma galactose concentrations with GAL + GLU [0.4 mmol.L; 95% confidence limits (CL): 0.1, 0.6] were lower (contrast: 0.5 mmol.L; 95% CL: 0.2, 0.8; P < 0.0001) than when GAL alone (0.9 mmol.L; 95% CL: 0.7, 1.2) was ingested. Exogenous carbohydrate oxidation with GAL alone (0.31 g·min−1; 95% CL: 0.28, 0.35) was marginally reduced (contrast: 0.05 g·min−1; 95% CL: −0.09, 0.00007; P = 0.01) when combined with glucose (GAL* + GLU 0.27 g·min−1; 0.24, 0.30). Total combined exogenous-carbohydrate oxidation (COMBINE: 0.57 g·min−1; 95% CL: 0.49, 0.64) was similar (contrast: 0.02 g·min−1; 95% CL: −0.05, 0.09; P = 0.63) when compared with isoenergetic GLU (0.55 g·min−1; 95% CL: 0.52, 0.58). In conclusion, coingestion of glucose and galactose did not enhance exogenous galactose oxidation during exercise. When combined, isoenergetic galactose-glucose ingestion elicited similar exogenous-carbohydrate oxidation to glucose suggesting galactose-glucose blends are a valid alternative for glucose as an exogenous-carbohydrate source during exercise. NEW & NOTEWORTHY Glucose and galactose coingestion blunted the galactosemia seen with galactose-only ingestion during exercise. Glucose and galactose coingestion did not enhance the oxidation of ingested galactose during exercise. Combined galactose-glucose (1:1 ratio) ingestion was oxidized to a similar extent as isoenergetic glucose-only ingestion during exercise. Galactose-glucose blends are a viable exogenous carbohydrate energy source for ingestion during exercise.fals

    A role for β-catenin in diet-induced skeletal muscle insulin resistance.

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    A central characteristic of insulin resistance is the impaired ability for insulin to stimulate glucose uptake into skeletal muscle. While insulin resistance can occur distal to the canonical insulin receptor-PI3k-Akt signaling pathway, the signaling intermediates involved in the dysfunction are yet to be fully elucidated. β-catenin is an emerging distal regulator of skeletal muscle and adipocyte insulin-stimulated GLUT4 trafficking. Here, we investigate its role in skeletal muscle insulin resistance. Short-term (5-week) high-fat diet (HFD) decreased skeletal muscle β-catenin protein expression 27% (p = 0.03), and perturbed insulin-stimulated β-cateninS552 phosphorylation 21% (p = 0.009) without affecting insulin-stimulated Akt phosphorylation relative to chow-fed controls. Under chow conditions, mice with muscle-specific β-catenin deletion had impaired insulin responsiveness, whereas under HFD, both mice exhibited similar levels of insulin resistance (interaction effect of genotype × diet p < 0.05). Treatment of L6-GLUT4-myc myocytes with palmitate lower β-catenin protein expression by 75% (p = 0.02), and attenuated insulin-stimulated β-catenin phosphorylationS552 and actin remodeling (interaction effect of insulin × palmitate p < 0.05). Finally, β-cateninS552 phosphorylation was 45% lower in muscle biopsies from men with type 2 diabetes while total β-catenin expression was unchanged. These findings suggest that β-catenin dysfunction is associated with the development of insulin resistance.fals

    Effects of Whey Protein on Skeletal Muscle Microvascular and Mitochondrial Plasticity Following 10-Weeks of Exercise Training in Men with Type-2 Diabetes

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    Copyright remains with the author(s) or their institution(s).Abstract Skeletal muscle microvascular dysfunction and mitochondrial rarefaction feature in type 2 diabetes mellitus (T2DM) linked to low tissue glucose disposal rate (GDR). Exercise training and milk protein supplementation independently promote microvascular and metabolic plasticity in muscle associated with improved nutrient delivery, but combined effects are unknown. In a randomised-controlled trial, 24 men (55.6 y, SD 5.7) with T2DM ingested whey protein drinks (protein/carbohydrate/fat: 20/10/3 g; WHEY) or placebo (carbohydrate/fat: 30/3 g; CON) before/after 45 mixed-mode intense exercise sessions over 10 weeks, to study effects on insulin-stimulated (hyperinsulinemic clamp) skeletal-muscle microvascular blood flow (mBF) and perfusion (near-infrared spectroscopy), and histological, genetic, and biochemical markers (biopsy) of microvascular and mitochondrial plasticity. WHEY enhanced insulin-stimulated perfusion (WHEY-CON 5.6%; 90% CI −0.1, 11.3), while mBF was not altered (3.5%; −17.5, 24.5); perfusion, but not mBF, associated (regression) with increased GDR. Exercise training increased mitochondrial (range of means: 40%–90%) and lipid density (20%–30%), enzyme activity (20%–70%), capillary:fibre ratio (∼25%), and lowered systolic (∼4%) and diastolic (4%–5%) blood pressure, but without WHEY effects. WHEY dampened PGC1α −2.9% (90% compatibility interval: −5.7, −0.2) and NOS3 −6.4% (−1.4, −0.2) expression, but other messenger RNA (mRNA) were unclear. Skeletal muscle microvascular and mitochondrial exercise adaptations were not accentuated by whey protein ingestion in men with T2DM. ANZCTR Registration Number: ACTRN12614001197628. Novelty: • Chronic whey ingestion in T2DM with exercise altered expression of several mitochondrial and angiogenic mRNA. • Whey added no additional benefit to muscle microvascular or mitochondrial adaptations to exercise. • Insulin-stimulated perfusion increased with whey but was without impact on glucose disposal. Résumé Le dysfonctionnement microvasculaire du muscle squelettique et la raréfaction mitochondriale caractérisant le diabète de type 2 (« T2DM ») sont liés à un faible taux d’élimination du glucose tissulaire (« GDR »). L’entraînement physique et la supplémentation en protéines du lait favorisent indépendamment la plasticité microvasculaire et métabolique dans le muscle; cette plasticité est associée à une amélioration de l’apport de nutriments, mais les effets combinés sont inconnus. Dans un essai contrôlé randomisé, 24 hommes (55,6 ans, SD 5,7) aux prises avec le T2DM consomment des boissons protéinées de lactosérum (protéines / glucides / lipides: 20/10/3 g; « WHEY ») ou un placebo (glucides / lipides: 30/3 g; « CON ») avant / après 45 séances d’exercice intense en mode mixte sur 10 semaines, et ce, pour examiner les effets sur le flux sanguin microvasculaire (« mBF ») et la perfusion (spectroscopie proche infrarouge) stimulés par l’insuline (clamp hyperinsulinémique), des variables histologiques, génétiques et des marqueurs biochimiques (biopsie) de la plasticité microvasculaire et mitochondriale. WHEY améliore la perfusion stimulée par l’insuline (WHEY-CON 5,6 %; IC 90 % −0,1, 11,3), tandis que le mBF n’est pas modifié (3,5 %; −17,5, 24,5); la perfusion, mais pas le mBF, est associée (régression) à une augmentation du GDR. L’entraînement à l’exercice augmente la densité mitochondriale (gamme de moyennes: 40-90 %) et lipidique (20−30 %), l’activité enzymatique (20−70 %), le ratio capillaire: fibre (∼25 %) et diminue les pressions systolique (∼4 %) et diastolique (4−5 %), mais sans effets de WHEY. WHEY amortit l’expression de PGC1α −2,9 % (intervalle de compatibilité de 90 % : −5,7, −0,2) et NOS3 −6,4 % (−1,4, −0,2), mais les autres ARN messager (ARNm) ne sont pas clairs. Les adaptations microvasculaires et mitochondriales des muscles squelettiques causées par l’entraînement physique ne sont pas accentuées par la consommation de protéines de lactosérum chez les hommes aux prises avec le T2DM. Numéro d’enregistrement ANXCTR : ACTRN12614001197628. [Traduit par la Rédaction] Les nouveautés: • La consommation prolongée de lactosérum en présence de T2DM combinée à l’entraînement physique modifie l’expression de plusieurs ARNm mitochondriaux et angiogéniques. • Le lactosérum n’ajoute aucun avantage supplémentaire aux adaptations microvasculaires ou mitochondriales musculaires à l’exercice physique. • La perfusion stimulée par l’insuline augmente avec le lactosérum mais n’a pas d’impact sur l’élimination du glucose.falseGaffney, Kim Lucero, Adam Macartney-Coxson, Donia Clapham, Jane Whitfield, Patricia Palmer, Barry Wakefield, StJohn Faulkner, James Stoner, Lee Rowlands, David Stephen eng Canada Appl Physiol Nutr Metab. 2021 Feb 16. doi: 10.1139/apnm-2020-0943. Skeletal muscle microvascular dysfunction and mitochondrial rarefaction feature in type-2 diabetes mellitus (T2DM) linked to low tissue glucose disposal rate (GDR). Exercise training and milk protein supplementation independently promote microvascular and metabolic plasticity in muscle associated with improved nutrient delivery, but combined effects are unknown. In a randomised-controlled trial, 24 men (55.6 y, SD5.7) with T2DM ingested whey protein drinks (protein/carbohydrate/fat: 20/10/3 g; WHEY) or placebo (carbohydrate/fat: 30/3 g; CON) before/after 45 mixed-mode intense exercise sessions over 10 weeks, to study effects on insulin-stimulated (hyperinsulinemic clamp) skeletal-muscle microvascular blood flow (mBF) and perfusion (near-infrared spectroscopy), and histological, genetic, and biochemical markers (biopsy) of microvascular and mitochondrial plasticity. WHEY enhanced insulin-stimulated perfusion (WHEY-CON 5.6%; 90%CI -0.1, 11.3), while mBF was not altered (3.5%; -17.5, 24.5); perfusion, but not mBF, associated (regression) with increased GDR. Exercise training increased mitochondrial (range of means: 40-90%) and lipid density (20-30%), enzyme activity (20-70%), capillary:fiber ratio (~25%), and lowered systolic (~4%) and diastolic (4-5%) blood pressure, but without WHEY effects. WHEY dampened PGC1alpha -2.9% (90%CI -5.7, -0.2) and NOS3 -6.4% (-1.4, -0.2) expression, but other mRNA were unclear. Skeletal muscle microvascular and mitochondrial exercise adaptations were not accentuated by whey protein ingestion in men with T2DM. Clinical Trial Registration Number: ACTRN12614001197628 Novelty Bullets: * Chronic whey ingestion in T2DM with exercise altered expression of several mitochondrial and angiogenic mRNA. * Whey added no additional benefit to muscle microvascular or mitochondrial adaptations to exercise. * Insulin-stimulated perfusion increased with whey but was without impact on glucose disposal

    Development of guidelines for giving community presentations about eating disorders: a Delphi study

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    Background: Concerns exist around how to talk about eating disorders (EDs) due to evidence that suggests discussing ED symptoms and behaviours may cause or worsen symptoms in vulnerable people. Using expert consensus, we developed a set of guidelines for giving safe community presentations about EDs. Methods: Participants with professional ED expertise, and people with lived experience of an ED, were recruited for a Delphi study. N = 26 panel members rated 367 statements for both a) inclusion in guidelines, and b) their potential to be helpful (increase knowledge, reduce stigma) or harmful (increase stigma, cause/worsen ED symptoms). After each round of the study, statements were classified as endorsed, re-rate, or not endorsed. Results: 208 statements were endorsed by the panel over three rounds. 13 statements were strongly endorsed in the first round, with both people with lived experience and professionals agreeing it is important for presentations to include information on etiology of EDs and to promote help-seeking. Several statements had a high level of disagreement between those with lived experience and professionals, including the idea that presentations should suggest dieting is likely to result in weight gain. Discussion: The experts were able to develop consensus on a wide range of issues. Panel members, particularly people with lived experience, were sensitive to aspects of presentations that may be harmful to an audience. The guidelines fill an important gap in the literature and provide guidance to those educating the public about EDs; they should, however, be further evaluated to test their efficacy

    The short-term effect of high versus moderate protein intake on recovery after strength training in resistance-trained individuals

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    Background: Dietary protein intakes up to 2.9 g.kg-1.d-1 and protein consumption before and after resistance training may enhance recovery, resulting in hypertrophy and strength gains. However, it remains unclear whether protein quantity or nutrient timing is central to positive adaptations. This study investigated the effect of total dietary protein content, whilst controlling for protein timing, on recovery in resistance trainees. Methods: Fourteen resistance-trained individuals underwent two 10-day isocaloric dietary regimes with a protein content of 1.8 g.kg-1.d-1 (PROMOD) or 2.9 g.kg-1.d-1 (PROHIGH) in a randomised, counterbalanced, crossover design. On days 8-10 (T1-T3), participants undertook resistance exercise under controlled conditions, performing 3 sets of squat, bench press and bent-over rows at 80% 1 repetition maximum until volitional exhaustion. Additionally, participants consumed a 0.4 g.kg-1 whey protein concentrate/isolate mix 30 minutes before and after exercise sessions to standardise protein timing specific to training. Recovery was assessed via daily repetition performance, muscle soreness, bioelectrical impedance phase angle, plasma creatine kinase (CK) and tumor necrosis factor-α (TNF-α). Results: No significant differences were reported between conditions for any of the performance repetition count variables (p>0.05). However, within PROMOD only, squat performance total repetition count was significantly lower at T3 (19.7 ± 6.8) compared to T1 (23.0 ± 7.5; p=0.006). Pre and post-exercise CK concentrations significantly increased across test days (p≤0.003), although no differences were reported between conditions. No differences for TNF-α or muscle soreness were reported between dietary conditions. Phase angle was significantly greater at T3 for PROHIGH (8.26 ± 0.82°) compared with PROMOD (8.08 ± 0.80°; p=0.012). Conclusions: When energy intake and peri-exercise protein intake was controlled for, a short term PROHIGH diet did not improve markers of muscle damage or soreness in comparison to a PROMOD approach following repeated days of intensive training. Whilst it is therefore likely that protein intakes (1.8g.kg-1.d-1) may be sufficient for resistance-trained individuals, it is noteworthy that both lower body exercise performance and bioelectrical phase angle were maintained with PROHIGH. Longer term interventions are warranted to determine whether PROMOD intakes are sufficient during prolonged training periods or when extensive exercise (e.g. training twice daily) is undertaken

    Postexercise muscle glycogen synthesis with glucose, galactose, and combined galactose-glucose ingestion.

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    Ingested galactose can enhance postexercise liver glycogen repletion when combined with glucose but effects on muscle glycogen synthesis are unknown. In this double-blind randomized study participants [7 men and 2 women; V̇o2max: 51.1 (8.7) mL·kg-1·min-1] completed three trials of exhaustive cycling exercise followed by a 4-h recovery period, during which carbohydrates were ingested at the rate of 1.2 g·kg-1·h-1 comprising glucose (GLU), galactose (GAL) or galactose + glucose (GAL + GLU; 1:2 ratio). The increase in vastus lateralis skeletal-muscle glycogen concentration during recovery was higher with GLU relative to GAL + GLU [contrast: +50 mmol·(kg DM)-1; 95%CL 10, 89; P = 0.021] and GAL [+46 mmol·(kg DM)-1; 95%CL 8, 84; P = 0.024] with no difference between GAL + GLU and GAL [-3 mmol·(kg DM)-1; 95%CL -44, 37; P = 0.843]. Plasma glucose concentration in GLU was not significantly different vs. GAL + GLU (+ 0.41 mmol·L-1; 95%CL 0.13, 0.94) but was significantly lower than GAL (-0.75 mmol·L-1; 95%CL -1.34, -0.17) and also lower in GAL vs. GAL + GLU (-1.16 mmol·-1; 95%CL -1.80, -0.53). Plasma insulin was higher in GLU + GAL and GLU compared with GAL but not different between GLU + GAL and GLU. Plasma galactose concentration was higher in GAL compared with GLU (3.35 mmol·L-1; 95%CL 3.07, 3.63) and GAL + GLU (3.22 mmol·L-1; 95%CL 3.54, 2.90) with no difference between GLU + GAL (0.13 mmol·L-1; 95%CL -0.11, 0.37) and GLU. Compared with galactose or a galactose + glucose blend, glucose feeding was more effective in postexercise muscle glycogen synthesis. Comparable muscle glycogen synthesis was observed with galactose-glucose coingestion and exclusive galactose-only ingestion. NEW & NOTEWORTHY Postexercise galactose-glucose coingestion or exclusive galactose-only ingestion resulted in a lower rate of skeletal-muscle glycogen replenishment compared with exclusive glucose-only ingestion. Comparable muscle glycogen synthesis was observed with galactose-glucose coingestion and exclusive galactose-only ingestion.fals
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